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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oligodendrogliomas (OD) are rare, diffusely infiltrating tumors, arising in the white matter of cerebral hemispheres, and displaying better sensitivity to treatment and prognosis than other gliomas. Favorable prognostic factors are low-grade, combined loss of 1p/19q, younger age, good performance status, and frontal localization. Low-grade OD usually present with seizures, whereas high-grade tumors often present with focal deficits, increased intracranial pressure or cognitive deficits. Treatment may be deferred until progression in young patients with low-grade OD presenting with seizures only. Patients with enhancing lesions, mass effect, focal deficits or increased intracranial pressure should be treated without delay. Treatment consists of resection as extensive and as safe possible. Postoperative radiotherapy is indicated for large, unresectable, or incompletely resected tumors; focal deficits; anaplastic tumors; or enhancing lesions. Adjuvant PCV chemotherapy increased progression-free survival but does not improve survival as compared to PCV given at recurrence. Chemotherapy with either PCV or temozolomide constitutes a standard for recurrent/progressive disease.
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PMID:Oligodendroglioma. 1827 88

Today, treatment recommendations for patients with all types of gliomas are based on light microscopic evaluation of tumor tissue with no allowance for genetic variability. Oligodendrogliomas are treated in a uniform manner with, as yet, no unique therapeutic approach or targeted therapy for those harboring a codeletion of chromosomes 1p and 19q. Surgical resection and radiotherapy are the standards-of-care for patients with oligodendrogliomas. Surgery improves symptoms, especially headache or seizures, and radiotherapy controls tumor growth for most patients. By extrapolation from randomized trials of glioblastoma, radiotherapy likely prolongs survival. Uncertainties persist about the timing of radiotherapy in the management of patients with low-grade oligodendrogliomas, but a superior antitumor treatment has yet to emerge. That said, the recognition that oligodendrogliomas with 1p/19q loss are sensitive to current therapies and slowly growing is already influencing our management of patients with this type of glioma, spawning trials in which patients are selected by molecular signature.
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PMID:Gliomas with 1p/19q codeletion: a.k.a. oligodendroglioma. 1906 May 98

A 10-yr-old female lion (Panthera leo) presented for acute onset ataxia and weakness with a history of two seizure episodes 6 mo prior to presentation and a persistent head tilt for at least 6 mo. Gross necropsy findings included a gelatinous mass in the right cerebral hemisphere extending from the frontal to the occipital lobes. Histologically, the mass was composed of polygonal cells surrounding lakes of mucinous material. These cells had clear cytoplasm, ovoid basophilic nuclei, and inapparent cell processes. Immunoreactivity was positive for S100 and neuron-specific enolase but negative for glial fibrillary acid protein, myelin basic protein, neurofilament triplet, vimentin, and cytokeratin. All findings were consistent with an oligodendroglioma. A second neoplasm, a pulmonary adenoma, was also iidentified at necropsy.
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PMID:Oligodendroglioma in an african lion (Panthera leo). 1911 Jul 12

Direct electrical stimulation of functional cortical areas is a standard procedure in epilepsy and glioma surgery. Many previous studies support that stimulation of the motor cortex with short-train pulses is a less epileptogenic alternative to the 50-60Hz 'Penfield' technique. However, whether the short-train stimulation is useful also in mapping of speech areas is unclear. In this case report we present a patient with oligodendroglioma near the Broca area. Extraoperative electrical stimulation via a subdural grid electrode was primarily performed to locate the speech area. The cortex was stimulated with short-train pulses (5 pulses, 0.5 pulse duration and 3ms interpulse interval) in addition to 1-3s 50Hz stimulation. The patient had speech arrest from both types of stimulation techniques during a naming task. It was however critical that the short (14.5ms) train stimulation was synchronized with the presentation of the naming objects. If not, there was no speech arrest. Despite this possible pitfall, this case has encouraged us to further try short-train stimulation in attempts to reduce stimulus-triggered seizures during mapping of eloquent areas.
Seizure 2009 Jun
PMID:Successful localization of the Broca area with short-train pulses instead of 'Penfield' stimulation. 1920 Dec 12

We report on a case of epilepsia partialis continua with rapid response to intravenous bolus administration of levetiracetam. A 60-year-old woman presented with continuous jerking of the right foot and hallux persisting for more than two days. She had a 9-year history of epilepsy due to a left temporoparietal oligodendroglioma with occasional focal seizures clinically presenting as speech arrest, which was treated with levetiracetam and oxcarbazepine administered orally. After hospital admission, the twitching of the foot and toe was refractory to add-on treatment with lorazepam and diazepam but stopped within 15 min after intravenous bolus administration of 2000 mg levetiracetam. This observation suggests that intravenous bolus administration of levetiracetam may be an effective therapeutic option in epilepsia partialis continua.
Seizure 2009 Dec
PMID:Epilepsia partialis continua responsive to intravenous levetiracetam. 1983 63

We describe the case of a 45-year-old woman with frequent simple partial seizures consisting mainly of autonomic manifestations including flatulence. The ictal onset and interictal EEG epileptiform abnormalities were localized to the right frontotemporal region. This localization was supported by structural brain imaging showing recurrence of a right frontotemporal oligodendroglioma with involvement of the insula. We therefore suggest that ictal flatulence is one of several autonomic and gastrointestinal symptoms and signs that may be used clinically in lateralizing to the nondominant hemisphere.
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PMID:Ictal flatulence: seizure onset in the nondominant hemisphere. 1984 45

Tourette syndrome is generally considered to be a genetic disorder, but symptoms mimicking Tourette syndrome can be secondary to an underlying lesion disrupting the basal ganglia circuitry. Described here is a case of secondary tics, or tourettism, in a child with a large oligodendroglioma of the right temporal lobe extending to the basal ganglia. He presented with attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and stimulant-induced tic disorder at the age of 11 years, and later also had also seizures. The family history was unremarkable. Cranial magnetic resonance imaging disclosed a right temporal lobe tumor extending to the basal ganglia. An alpha-[(11)C]methyl-l-tryptophan positron emission tomography scan showed asymmetric uptake in the basal ganglia and intense uptake in the tumor. He had a lesionectomy, and the histopathologic diagnosis was oligodendroglioma. Neuropsychologic testing after surgery revealed no attention-deficit hyperactivity disorder symptomatology, and only minimal features of obsessive-compulsive disorder. The present case provides additional evidence supporting the role of basal ganglia circuitry in the pathophysiology of tic disorder and its comorbid states. Children who present with attention-deficit hyperactivity disorder, obsessive-compulsive disorder, and tic disorder of late onset in the absence of family history should be further investigated with neuroimaging to exclude the presence of a secondary cause.
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PMID:Secondary tics or tourettism associated with a brain tumor. 1993 Nov 71

We report a 37-year-old man with a primary intracranial oligodendroglioma presenting later with symptomatic multiple cerebrospinal fluid (CSF) intradural drop spinal metastases. This patient initially presented in 2006 with complex partial seizures. Initial histology demonstrated World Health Organization (WHO) grade 2 oligodendroglioma. The patient had further generalised seizures 7 months after initial tumour resection. MRI at that time confirmed tumour recurrence. The patient underwent a repeat craniotomy. Histology showed anaplastic transformation to a WHO grade 3 oligodendroglioma. About 30 months after his initial presentation, the patient developed a focal neurological deficit in the left leg with associated retention of urine. MRI of the neuraxis demonstrated widespread leptomeningeal metastatic drop deposits within the spinal canal. We discuss the mechanisms involved in tumour dissemination throughout the CSF. We also review the relevant literature regarding this phenomenon.
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PMID:Oligodendroglioma presenting with intradural spinal metastases: an unusual cause of cauda equina syndrome. 2004 38

Synaptic vesicle protein 2A (SV2A) has been identified as the binding site for the antiepileptic drug levetiracetam and is thought to decrease neuronal excitability. Since knockout of SV2A in mice leads to seizures, we hypothesized that a reduction in SV2A expression promotes seizure generation in epilepsy-associated brain tumors. We compared the SV2A expression and distribution in surgically removed tumor tissue (n = 63) and peritumoral cortex (n = 31) of patients with glial and glioneuronal tumors to normal control cortex obtained at autopsy in nonbrain tumor patients (n = 6). Additionally, we compared the SV2A expression and distribution in tumor patients with epilepsy (n = 39) with SV2A expression in tumor patients without epilepsy (n = 24). Immunohistochemistry in control cortex demonstrated strong and diffuse SV2A immunoreactivity (IR) throughout all cortical layers. Similar strong SV2A IR (with the same diffuse distribution pattern) was observed in the peritumoral cortical specimens in both patients with and without epilepsy. Modest SV2A IR was observed within the tumor area. The SV2A-positive cells detected within the tumor area were mainly entrapped neurons. Oligodendrogliomas and glioneuronal tumors displayed variable SV2A neuropil staining. In ganglioglioma (GG), strong SV2A IR was present along the dysplastic neuronal cell borders and processes. In both GG and dysembryoplastic neuroepithelial tumors, SV2A IR was occasionally observed within the neuronal perikarya. We found no differences in SV2A expression in the peritumoral cortex between the patients with and without epilepsy, which suggests that the role of SV2A in epileptogenesis in patients with glial tumors is questionable. The distinct pattern of SV2A IR in glioneuronal tumors suggests a redistribution of SV2A.
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PMID:Expression of synaptic vesicle protein 2A in epilepsy-associated brain tumors and in the peritumoral cortex. 2016 14

Various subtypes of intracerebral hamartomas, associated with seizure disorders, have long been described. We describe a cerebral hamartoma placed in the left frontal lobe, associated with drug-resistant epilepsy, composed exclusively of mature oligodendroglial cells. The patient was a 27-year-old right-handed male presenting with severe epileptic encephalopathy and symptoms of behavior dysfunction (disinhibition, rage attacks) associated with a left frontal lesion. Magnetic resonance imaging revealed a small area iso-hypointense compared to the gray matter in T1-weighted sequences not enhancing after gadolinium contrast injection in the left frontal site. On histology, a cortical lesion composed of large aggregates of oligodendroglial cells, with round central nuclei and clear perinuclear halos, was observed. Neither mitotic figures nor necrosis were present. Reactivity for Ki67 and P53 was not found. The lesion was well demarcated from the adjacent brain parenchyma and perineuronal satellitosis was not observed in the cortex. In conclusion, albeit extremely rare, recognition of oligodendroglial hamartoma and its distinction from other epileptogenic lesions as dysembryoplastic neuroepithelial tumor or above all oligodendroglioma have important therapeutic and prognostic implications.
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PMID:Oligodendroglial hamartoma: a potential source of misdiagnosis for oligodendroglioma. 2053 10


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